The aortic valve in the human heart is a one-way valve that separates the left ventricle from the aorta. The aorta is a large artery that carries oxygen-rich blood out of the left ventricle to the rest of the body. Aortic insufficiency is a condition in which the aortic valve does not fully close during ventricular diastole, thereby allowing blood to flow backward from the aorta into the left ventricle. This leakage of blood through the aortic valve back into the left ventricle is often referred to as aortic valve regurgitation.
Aortic insufficiency is typically caused by aortic root dilatation (annuloaortic ectasia), which is idiopathic in over 80% of the cases. Aortic insufficiency may also result from other factors, such as aging and hypertension. In any case, the regurgitation of blood resulting from aortic insufficiency substantially reduces the pumping efficiency of the left ventricle. Therefore, even during periods of rest, the heart must work hard simply to maintain adequate circulation through the body. Over time, this continuous strain on the heart can damage the left ventricle. For example, the additional strain on the heart may result in a thickening of the heart muscle (hypertrophy). When heart-wall thickening occurs due to aortic insufficiency, the geometry of the heart can be adversely affected and the heart can be permanently damaged.
Although aortic insufficiency is relatively common, the treatment of this condition still represents a substantial clinical challenge for surgeons and cardiologists. For example, because aortic insufficiency has a long latency period, afflicted patients may already be at significant risk for heart failure by the time the symptoms arise. In many cases, when patients are not monitored well for aortic insufficiency and are left untreated, the patient's left ventricle may become irreversibly damaged before therapy can be delivered. Therefore, even if a defective aortic valve is replaced with a prosthetic valve, the patient may never fully recover and their survival rate may be substantially impaired.
Existing methods of treating aortic insufficiency suffer from a number of significant disadvantages. For example, open heart surgical valve replacement is often too traumatic for older and/or frail individuals. Replacement of the aortic valve using existing catheterization techniques is also challenging because it is difficult to anchor a prosthetic valve within a soft and dilated annulus. More particularly, when a prosthetic valve is delivered to the site of the aortic valve and expanded, it engages and continuously exerts an outward force against the aortic valve wall. This continuous outward pressure is necessary for anchoring the prosthetic valve within the native valve but may also cause the already-dilated native aortic annulus to become further expanded. The tissue along the annulus of a valve suffering from aortic insufficiency is typically soft and flexible (as opposed to being hard and calcified as with aortic stenosis) and therefore the further expansion of the aortic annulus may lead to dislodgement of the prosthetic valve. Such dislodgement could require delivery of a still larger valve or result in death of the patient. A prosthetic valve with a very large diameter may be delivered via a catheterization technique to reduce the possibility of dislodgement. However, it follows that such a valve would also have a large diameter in its crimped condition. The delivery of such a large-diameter prosthetic valve is much more challenging and dangerous than the delivery of a relatively small prosthetic valve of the type currently used to treat aortic stenosis.
Therefore, a need exists for new and improved methods and devices for treating aortic insufficiency.